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Biomedical subjects

M T Pieraggi

Publications and source records attributed to M T Pieraggi.

At least 73 records · Page 4Linked to original sources
PubMed1981

[Macroglobulinemia (Waldenström) with specific cutaneous nodules (author's transl)].

The authors present a case of Waldenström's disease in a 68-year-old woman. The only symptoms were several nodes on the leg. The pathological, and immunological finding showed the presence of lymphoplasmocytic cells in the middle dermis; there was a positive reaction with the anti-IgM serum. Ultrastructural studies showed large cells with dilated reticulum and abnormal IgM globulin was found in the serum in large amounts. The rate of the others immunoglobulins was normal. There was a lymphoplasmocytic proliferation in the bone medullar. The specific cutaneous manifestation of the Waldenström's disease are 1) large "plaques" or/and 2) nodes. The pathological studie shows numerous lymphoplasmocytic or immunoblastic cells and sometimes the presence of an amorphous material which is the abnormal globulin.

Aged↗
PubMed1981

[Human aorta: endothelium and atheroma (author's transl)].

An electron microscopic study of aortic endothelium obtained from necropsy and biopsy material shows pathological changes corresponding the severity of the atheromatous state, but unrelated to age. All stage I aortas show the same type of endothelial changes. So do stage II aortas. The pathological structural changes in the endothelial cells corresponding to aortas of stage I, II-III involve the microfilaments, vesicles, intercellular junctions and basement membrane. The microfilaments are more numerous and better defined in atheromatous aortas. Also rare bundles of microfilaments with electron-dense centers are seen. The intra-cytoplasmic vesicles increase presently deeper invaginations (pseudo-channels) in the stages II and III aortas. In these stages the intercellular junctions are open involving all or part of the junctions. All three described ultra-structural changes increase the permeability of the endothelium to lipids and plasma glycoproteins. The thickening of the sub-endothelial basement membrane résults from the increase of type IV collagen synthesized by the endothelial cells. Lysis of endothelial cells and platelet agregation are related to the stage of atheromatosis. The number of Weibel Palade bodies increase in stade II and III aortas. These organelles play a role in blood coagulation and accelerate atheromatosis. In conclusion, the aortic endothelium constitutes an active barrier. The pathological atheromatosis process involves the endothelium. The endothelial cells play a normal role in the passage of molecules from blood plasma into the aortic wall. That explains intimal formation and intimal fibrosis. The endothelium also participates in the initial pathogenic mechanism of atheroma formation (fatty dot and streak, gray gelatinous elevation and mural thrombus).

Aging↗
PubMed1980

Long term lathyrism and atherogenic diet in the rat. Protective action of pyridinol carbamate.

In the rat, prolonged administration (7 months) of Beta-Aminopropionitrile in association with a hyperlipidic diet caused the formation of widespread pronounced atheroma. The addition of Pyridinol Carbamate during the treatment minimized and retarded the appearance of lipid overload lesions. The histological modifications were found together with an increase in the free cholesterol fraction. These two observations explain the protective role of Pyridinol Carbamate on the wall of the aorta.

Aminopropionitrile↗
PubMed1980

Chronic lathyrism and atheromatosis in the rat. Protective effect of metformin.

Chronic administration of beta-aminopropionitrile fumarate (BAPN) (1 g/kg/day for 9 weeks) produced morphological changes of the aorta wall and in dermis, and biochemical changes of the aortic wall in the rat. Chronic administration of BAPN did not produce plasma lipid abnormalities such as those due to hyperlipidic diet. 9 weeks of BAPN followed by 10 months of a hyperlipidic diet increased the aortic cholesterol level and induced atheroma. The diet alone only produced an endothelial lipid overload and increased the aortic cholesterol level but less than BAPN and hyperlipidic diet together. Addition of metformin to BAPN prevented the formation of atheromatous lesions in the aorta and minimized the level of lipids in the aortic wall and of the dermis.

Aminopropionitrile↗
PubMed1980

Age dependent biochemical changes in dermal connective tissue. Relationship to histological and ultrastructural observations.

A biochemical study of skin biopsies of young normal subjects and two groups of aged subjects, one active and the other confined to bed, was made and the results compared with histological observations. Skin biopsies were incubated with 3H proline and 14C glucosamine and connective tissue components were sequentially extracted. In each extract the specific activity of total and collagenous protein was determined. With age a decrease was observed in both the amount of protein and the 3H proline incorporation of collagenous extracts. A parallel increase in 14C glucosamine incorporation was also noticed in extracts containing glycosaminoglycans and structural proteins. These results agree in part with the changes observed by light and electron microscopy, which revealed an increase in ground substance and fragmentation of collagen bundles in the dermis of older subjects.

Adult↗
PubMed1980

[Mammary Paget's disease: an ultrastructural study (author's transl)].

A case of mammary Paget's disease has been studied under electron microscopy. It seems that Paget's cells are coming from the basal layer which is not affected by the malignant proliferation. Paget's cells show some characters of keratinocytes such as rudimentary desmosomes and tonofilaments. But the tumoral tissue is very loose. The Paget's cells are not keratinised; they present numerous vesicles as malignant cells of apocrin mammary carcinoma. There are numerous histogenetic theories of Paget's disease. One of them sounds very interesting: it consists in looking for associations between microscopic mammary Paget's disease and mammary apocrin carcinoma.

Aged↗
PubMed1980

Mesangial isolated C3 deposition in patients with recurrent or persistent hematuria.

We reviewed 222 renal biopsies performed on patients with nonurologic hematuria alone or hematuria and proteinuria. This review revealed 31 patients who presented minor glomerular abnormalities with granular mesangial C3 deposition without any immunoglobulin or other complement component deposits. These patients presented with gross hematuria in five cases, microscopic hematuria alone in 12 cases, and proteinuria and microscopic hematuria in 14 cases. Light microscopy disclosed a segmentally increased mesangial matrix, sometimes associated with a segmental and focal mesangial hypercellularity. Focal tubulointerstitial and arteriolar lesions occurred in seven cases. In all cases, immunofluorescence showed diffuse granular mesangial deposition of C3. However, the deposits were not observed along the glomerular and tubular basement membranes. We should point out the high frequency of arteriolar C3 deposits (27 of 31). They were either isolated or associated with IgM or other complement components. Using electron microscopy, an increase of mesangial matrix and/or a proliferation of mesangial cells was observed. In two cases, electron-dense deposits were present in the mesangium. Glomerular basement membranes were normal in all but five cases, where they appeared segmentally thickened. After a 3-year follow-up study the clinical features remained unchanged.

Adolescent↗
PubMed1980

Chronic lathyrism. Plasma, aorta and rat skin treated for five months with beta-aminopropionitrile with or without high fat diet.

Previous experiments proved that white Wistar rats, resistant to spontaneous or experimental atheroma, present arteriosclerosis (parietal aorta lesions) and atheroma lesions (fat deposits) after a 9 week-treatment by Beta-aminopropionitrile (BAPN) followed by a high fat diet. The present work shows that BAPN alone, administered for 5 months, does not induced atheroma; its formation needs both lipid humoral disorders and parietal aortic lesions. It confirms certain facts noted in the aging of man and in the formation of atheroma.

Aminopropionitrile↗
PubMed1980

[Effect of pyridinol carbamate on long-term lathyrism and experimental atheroma in the rat. Histological and biochemical study].

Three-week-old rats were fed with Beta-aminopropionitrile (BAPN) with a normal or hyperlipidic diet. After a few weeks BAPN induced aortic elastic fibres disruption which as not worsened when the treatment was continued up the seven months. Adding a hyperlipidic diet produced atherosclerotic-like lesions. Pretreatment with Pyridinol Carbamate (PDC) whichever the diet used did not modify serum of aortic cholesterol levels. It decreased the severity of aortic lesions and delayed the onset of less severe atheromatous lesions. It seems that PDC increased the free/esterified aortic cholesterol ratio resulting in a better elimination of the aortic cholesterol.

Aminopropionitrile↗
PubMed1979

Fine structural evidence of increased endothelial permeability in chronic lathyrism.

The endothelium of the thoracic aorta of Wistar rats intoxicated with Beta-Aminopropionitrile (BAPN) for 9 weeks was studied. The animals were sacrificed at intervals, from the first to the 9th week of the treatment and 1, 2 and 3 months after the end of the treatment. Changes in the endothelial cells were studied by electron microscopy after staining with uranyl acetate and lead citrate, after impregnation with lanthanum. BAPN increased endothelial permeability, pinocytosis was more active in treated rats than controls, the intercellular junctions widened and cytoplasmic lesions with cell necrosis occurred. These intimal changes were comparable to those observed in man during ageing and in arteriosclerosis.

Animals↗
PubMed1979

Paracolloid of the skin.

A 51-year-old Caucasian man presented with a yellowish lesion containing multiple protuberances over his right cheek. Light and electron microscopic examination revealed an anhistic substance lacking definite characteristics of either amyloid or collid milium. The term paracolloid degeneration of the skin is introduced to designate this substance which is believed to derive from collagen. A review of the literature showed similar cases previously published under the names of nodular amyloidosis or disseminated colloid.

Amyloid↗
PubMed1978

Chronic lathyrism and atheromatosis in the rat. Study of the V.L.D.L. and plasma and arterial wall lipids.

Temporary chronic administration of Beta-amino-propionitrile (B.A.P.N.) produced morphological and biochemical changes of the aortic wall of rat as well as abnormalities of the plasma lipid levels. A hyperlipidic diet resulted in the blood plasma lipid abnormalities as B.A.P.N. intoxication. Nine weeks of B.A.P.N. followed by 42 weeks of a hyperlipidic diet increased the aortic cholesterol level and induced an atheroma. The diet alone produced only an endothelial lipid overload. The structure of arterial wall played the decisive role in atherogenesis.

Aminopropionitrile↗
PubMed1978

Hypothesis on microangiopathy of cutaneous capillaries.

Microangiopathy is a more or less pronounced PAS deposit-located exterior to the endothelial cells of the lymphatics and the basal membrane of the capillaries. This lesion, found in various normal and pathological states, has generated numerous pathogenic hypotheses. The presence of microangiopathy in 5 groups of 50 subjects representing five different clinical conditions, subjects over 60 years old or less than 40, diabetics, latent diabetics or patients with severe coronary heart disease, together with microscopic and/or ultrastructural lesions of the connective tissue (fibroblasts, collagen and elastic fibers, ground substance) has enabled us to propose a pathogenic hypothesis applicable to any microangiopathy. The initial change, hereditary or acquired, would be fibroblastic or interstitial. It would be characterized by the accumulation of glycoproteins, proteoglyacans and soluble collagen in the interstitium. Incomplete drainage of these macromolecules would occur around the blood and lymphatic capillaries and manifest itself by a PAS deposit, the hallmark of the microangiopathy.

Adult↗